Anti-PERK (phosphorylated and non phosphorylated) Antibody
Our Anti-PRKR-like endoplasmic reticulum kinase (phosphorylated and non phosphorylated) (PERK) rabbit polyclonal primary antibody detects mouse PRKR-like endoplasmic reticulum kinase (phosphorylated and non phosphorylated) (PERK), and is whole serum. It is validated for use in ICC, WB.
Western Blot using mouse cultured astrocyte extracts at rest (Cntrl) and after 60 mins of ER stress induction by oxygen glucose deprivation (OGD). The left panel membrane was probed with Rabbit polyclonal antibody to mouse PERK: Whole serum (R-1333-100). The right membrane was similarly probed in combination with the antigenic peptide used to generate the antibody. Image taken from Bollo et al (2010) Figure S4.
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SKU: R-1333-100
Ships: 1-2 business days
Product Details
PRKR-like endoplasmic reticulum kinase (phosphorylated and non phosphorylated) (PERK)
PERK (PKR-like ER kinase) is a single-pass type I ER membrane protein with a stress-sensing luminal domain connected by a transmembrane segment to a cytoplasmic-kinase domain.
Whole serum
Polyclonal
Mixed
ICC, WB
Rabbit
A recombinant peptide from mouse PERK.
Mouse
Mouse
Aliquot and store at -20°C for a higher stability. Avoid freeze-thaw cycles.
Liquid
50% glycerol
WB: 1:500
IP: 60 µg/mL
IP: 60 µg/mL
Unconjugated
This antiserum is known to recognize both phosphorylated and non phosphorylated mouse PERK.
For research use only.
United States
12 months after date of receipt (unopened vial).
Pek; Eukaryotic translation initiation factor 2-alpha kinase 3; PRKR-like endoplasmic reticulum kinase; pancreatic eIF2-alpha kinase; Eif2ak3; Perk
Q9Z2B5
UniProt Summary: Metabolic-stress sensing protein kinase that phosphorylates the alpha subunit of eukaryotic translation initiation factor 2 (EIF2S1/eIF-2-alpha) in response to various stress, such as unfolded protein response (UPR). Key effector of the integrated stress response (ISR) to unfolded proteins: EIF2AK3/PERK specifically recognizes and binds misfolded proteins, leading to its activation and EIF2S1/eIF-2-alpha phosphorylation. EIF2S1/eIF-2-alpha phosphorylation in response to stress converts EIF2S1/eIF-2-alpha in a global protein synthesis inhibitor, leading to a global attenuation of cap-dependent translation, while concomitantly initiating the preferential translation of ISR-specific mRNAs, such as the transcriptional activators ATF4 and QRICH1, and hence allowing ATF4- and QRICH1-mediated reprogramming. The EIF2AK3/PERK-mediated unfolded protein response increases mitochondrial oxidative phosphorylation by promoting ATF4-mediated expression of COX7A2L/SCAF1, thereby increasing formation of respiratory chain supercomplexes. In contrast to most subcellular compartments, mitochondria are protected from the EIF2AK3/PERK-mediated unfolded protein response due to EIF2AK3/PERK inhibition by ATAD3A at mitochondria-endoplasmic reticulum contact sites. In addition to EIF2S1/eIF-2-alpha, also phosphorylates NFE2L2/NRF2 in response to stress, promoting release of NFE2L2/NRF2 from the BCR(KEAP1) complex, leading to nuclear accumulation and activation of NFE2L2/NRF2. Serves as a critical effector of unfolded protein response (UPR)-induced G1 growth arrest due to the loss of cyclin-D1 (CCND1). Involved in control of mitochondrial morphology and function.
UniProt Summary: Metabolic-stress sensing protein kinase that phosphorylates the alpha subunit of eukaryotic translation initiation factor 2 (EIF2S1/eIF-2-alpha) in response to various stress, such as unfolded protein response (UPR). Key effector of the integrated stress response (ISR) to unfolded proteins: EIF2AK3/PERK specifically recognizes and binds misfolded proteins, leading to its activation and EIF2S1/eIF-2-alpha phosphorylation. EIF2S1/eIF-2-alpha phosphorylation in response to stress converts EIF2S1/eIF-2-alpha in a global protein synthesis inhibitor, leading to a global attenuation of cap-dependent translation, while concomitantly initiating the preferential translation of ISR-specific mRNAs, such as the transcriptional activators ATF4 and QRICH1, and hence allowing ATF4- and QRICH1-mediated reprogramming. The EIF2AK3/PERK-mediated unfolded protein response increases mitochondrial oxidative phosphorylation by promoting ATF4-mediated expression of COX7A2L/SCAF1, thereby increasing formation of respiratory chain supercomplexes. In contrast to most subcellular compartments, mitochondria are protected from the EIF2AK3/PERK-mediated unfolded protein response due to EIF2AK3/PERK inhibition by ATAD3A at mitochondria-endoplasmic reticulum contact sites. In addition to EIF2S1/eIF-2-alpha, also phosphorylates NFE2L2/NRF2 in response to stress, promoting release of NFE2L2/NRF2 from the BCR(KEAP1) complex, leading to nuclear accumulation and activation of NFE2L2/NRF2. Serves as a critical effector of unfolded protein response (UPR)-induced G1 growth arrest due to the loss of cyclin-D1 (CCND1). Involved in control of mitochondrial morphology and function.
13666
2-8°C (on cold packs)

